PMID- 25329633
OWN - NLM
STAT- MEDLINE
DCOM- 20150629
LR  - 20141021
IS  - 1399-0039 (Electronic)
IS  - 0001-2815 (Linking)
VI  - 84
IP  - 5
DP  - 2014 Nov
TI  - Genetic risk for co-occurrence of type 1 diabetes and celiac disease is modified 
      by HLA-C and killer immunoglobulin-like receptors.
PG  - 471-8
LID - 10.1111/tan.12450 [doi]
AB  - The prevalence of celiac disease (CD) in patients with type 1 diabetes (T1D) has 
      been reported to be 5-7 times higher than in the general population. Risk factors 
      for co-occurrence of both diseases have not been entirely established. The aim of 
      our study was to analyze possible impact of human leukocyte antigen (HLA) class I 
      and killer cell immunoglobulin-like receptors (KIRs) on the co-occurrence of T1D 
      and CD. We analyzed 67 patients with T1D, 68 patients with CD, 69 patients with 
      both diseases (T1D+CD) and 130 controls. Statistical analysis was based on two 
      tailed Fisher exact test with corrections for multiple testing. After 
      stratification by DR3-DQ2, an association of HLA class I part of the COX 
      haplotype (A1-B8-Cw7-DR3-DQ2) was not observed with each of the studied diseases 
      separately, but it could be shown in case of the co-occurrence of T1D and CD. 
      Only in the group of patients with coexisting diseases, the presence of HLA-C*07 
      (P = 8.65x10(-3) ) and HLA-B*08 (P = 0.03) but not HLA-A*01 increased the 
      succeptibility. Our current data indicated that C*07, contributing C1 ligand (Pc 
       = 3.67x10(-5) ) rather than B*08, that possesses no KIR ligand, could have an 
      impact on the innate immunity rout of this susceptibility. The significant 
      combination of C1-KIR2DL3 (Pc  = 1.97x10(-4) ) observed in patients with 
      coexisting diseases supports this hypotesis. Interestingly, no association was 
      observed when C1 in combination with its stronger inhibitory receptor KIR2DL2 was 
      investigated. Predominantly, weak inhibition in patients with coexisting T1D and 
      CD could lead to a natural killer cell response, making them vulnerable for 
      developing more than one autoimmune disease.
CI  - (c) 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Smigoc Schweiger, D
AU  - Smigoc Schweiger D
AD  - Department of Pediatric Endocrinology, Diabetes and Metabolic Diseases, 
      University Medical Centre - University Children's Hospital, Ljubljana, Slovenia.
FAU - Mendez, A
AU  - Mendez A
FAU - Kunilo Jamnik, S
AU  - Kunilo Jamnik S
FAU - Bratanic, N
AU  - Bratanic N
FAU - Bratina, N
AU  - Bratina N
FAU - Battelino, T
AU  - Battelino T
FAU - Brecelj, J
AU  - Brecelj J
FAU - Vidan-Jeras, B
AU  - Vidan-Jeras B
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (HLA-C Antigens)
RN  - 0 (KIR2DL2 protein, human)
RN  - 0 (KIR2DL3 protein, human)
RN  - 0 (Receptors, KIR2DL2)
RN  - 0 (Receptors, KIR2DL3)
SB  - IM
MH  - *Celiac Disease/epidemiology
MH  - Comorbidity
MH  - *Diabetes Mellitus, Type 1/epidemiology/genetics
MH  - Female
MH  - *Genetic Predisposition to Disease
MH  - HLA-C Antigens/*genetics
MH  - Humans
MH  - Male
MH  - Prevalence
MH  - Receptors, KIR2DL2/*genetics
MH  - Receptors, KIR2DL3/*genetics
OTO - NOTNLM
OT  - celiac disease
OT  - co-occurrence
OT  - human leukocyte antigen class I
OT  - killer cell immunoglobulin-like receptor
OT  - receptor-ligand interaction
OT  - type 1 diabetes
EDAT- 2014/10/21 06:00
MHDA- 2015/06/30 06:00
CRDT- 2014/10/21 06:00
PHST- 2014/04/29 00:00 [received]
PHST- 2014/09/06 00:00 [revised]
PHST- 2014/09/12 00:00 [accepted]
PHST- 2014/10/21 06:00 [entrez]
PHST- 2014/10/21 06:00 [pubmed]
PHST- 2015/06/30 06:00 [medline]
AID - 10.1111/tan.12450 [doi]
PST - ppublish
SO  - Tissue Antigens. 2014 Nov;84(5):471-8. doi: 10.1111/tan.12450.